1. Field of the Invention
The present invention is directed to a method and apparatus for predicting the onset of a heart arrhythmia.
2. Background
Medical devices such as pacemakers and implantable cardioverter defibrillators (ICDs) monitor the electrical activity of a patient's heart and detect arrhythmias. Such devices monitor electrical activity in the atria, the ventricles, or both the atria and ventricles. Often such devices initiate some type of electrical therapy upon detection of an arrhythmia. For example, such devices may provide bradycardia pacing, antitachycardia pacing, cardioversion or defibrillation therapy.
A disadvantage of initiating treatment only upon detection of a rapid heart rate or tachyarrhythmia is that some treatments require a relatively lengthy preparation time. This is especially true of treatments for arrhythmias involving the ventricles of the heart, i.e. ventricular fibrillation or ventricular tachycardia, which are particularly dangerous and often fatal if not treated. For example, a typical treatment for ventricular fibrillation is to apply a high voltage shock to the heart. Generally, this involves precharging a capacitor, which can take as long as thirty seconds, thus delaying treatment for as long as thirty seconds following onset of the fibrillation. Medical devices that predict the onset of a heart arrhythmia would be advantageous by having therapy primed and ready for delivery at the onset of arrhythmia. It may also be possible to provide treatment to the heart that would prevent the onset of the arrhythmic event.
Many prior efforts to predict heart arrhythmias have focussed on long-term prediction of risk, that is, identifying people who are at risk of suffering heart arrhythmias and quantifying those risks. A common technique used in this long-term risk stratification is heart rate variability analysis derived from power spectral analysis of the heart's R--R intervals. The low frequency component of the power spectrum is attributed to the sympathetic input to the heart and the high frequency component is attributed to the respiratory cycle and vagal input. Decreased vagal tone is considered a marker for elevated arrhythmic risk. Recent efforts in short-term prediction of arrhythmias have centered on changes in electrogram features such as T wave alternans and patterns in the R--R intervals, or changes in the neural activity, similar to the techniques of long-term risk stratification. The instant invention looks instead at the morphology of the QRS complex recorded via an intracardiac electrode. The activation complex morphology is represented by the power spectrum of the complex and changes therein are analyzed to predict the onset of a heart arrhythmia.
The interest in QRS morphology changes is in part due to the work by K. Lund et al. showing cyclic variation in body surface electrogram morphology due to respiration. His work also alludes to direct neural input to the ventricular myocardium and cyclic variations at that level, which influence beat-to-beat morphology. It can be inferred that a decrease in neural input would influence the cyclic changes in morphology.